Higher animals establish host defense by orchestrating innate and adaptive immunity. This is mediated by professional antigen presenting cells, i.e. dendritic cells (DCs). DCs can incorporate pathogens, produce a variety of cytokines, maturate, and present pathogen-derived peptides to T cells, thereby inducing T cell activation and differentiation. These responses are triggered by microbial recognition through type I transmembrane proteins, Toll-like receptors (TLRs) on DCs. TLRs consist of ten members and each TLR is involved in recognizing a variety of microorganism-derived molecular structures. TLR ligands include cell wall components, proteins, nucleic acids, and synthetic chemical compounds, all of which can activate DCs as immune adjuvants. Each TLR can activate DCs in a similar, but distinct manner. For example, TLRs can be divided into subgroups according to their type I interferon (IFN) inducing ability. TLR2 cannot induce IFN-alpha or IFN-beta, but TLR4 can lead to IFN-beta production. Meanwhile, TLR3, TLR7, and TLR9 can induce both IFN-alpha and IFN-beta. Recent evidences suggest that cytoplamic adapters for TLRs are especially crucial for this functional heterogeneity. This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the C-terminal region of mouse TLR1.
The TLR1 gene is mapped to human chromosome 4p14. Tlr1 is widely expressed in several leukocytes and cells of myeloid lineage including monocytes, macrophages, and dendritic cells.
Immunogen
TLR1 (Q9EPQ1, 769-805) This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the C-terminal region of mouse TLR1.
Biochem/physiol Actions
The members of the TLR (toll-like receptor) family play important role in host-pathogen interaction by identifying specific molecular patterns in various microorganisms during early innate immune response. The immune and inflammatory responses against microbial infection or tissue injury is controlled by Tlrs by initiating signal cascades and in turn, promoting the secretion of cytokines and chemokines. Tlr1 might be involved in the regulation of mucosal immune response in gut, by forming a heterodimer with Tlr2. Apart from immune cells, TLRs are also expressed on tumor cells and stromal cells. The functional role of Tlr1 is not well understood, therefore, further elucidation is required for clarity over its underlying mechanism.
Physical form
Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.
Molecular cancer therapeutics, 15(7), 1740-1745 (2016-05-20)
The purpose of this study was to evaluate the clinical significance of single-nucleotide polymorphisms in TLR1, TLR2, TLR6, and TAK1 in patients with metastatic colorectal cancer (mCRC). We genotyped 9 SNPs of TLR1, TLR2, TLR6, and TAK1 in mCRC patients
Toll like receptors (TLR) are key elements of the innate immune response and involved in the recognition of pathogens. To test common and rare TLR variants involved in susceptibility or resistance to infection with Mycobacterium tuberculosis we screened the exons
Exposure to organic dust from agricultural environments is associated with inflammatory respiratory conditions. The putative causal agents in organic dust include viral, microbial and fungal components, which are recognized by the family of Toll-like receptors (TLRs) and drive host innate
Helicobacter pylori (H. pylori) -induced gastric inflammation impacts the functions of leptin- and ghrelin-producing cells in the gastroduodenum. Inflammation resulting from H. pylori sensing via Toll-like receptors (TLRs) and the associated downstream signaling largely remain ambiguous. Here, we investigated the
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